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However, the molecular bases of this phenomenon remain unclear. We report here a new mechanism to explain this threshold effect, based on a reserve of enzymes not initially participating in the respiratory rate that can be activated either to respond to a flux increase or to compensate for a defect induced by a mutation.
We show that this mobilization occurs through 1 the assembly of inactive adenine nucleotide translocator isoform 1 subunits into oligomeric active carriers or 2 conformational changes in the adenine nucleotide translocator isoform 1 in a permeability transition pore-like structure.
We discuss how these transitions are sensitive to the steady state of oxidative phosphorylation functioning or tissue and analyze their consequences on the threshold effect.
Consequently, impairments of mitochondrial function have been associated with the emergence of severe 20411 trainerhandbook disorders, known as mitochondrial cytopathies 12. Despite a broad characterization of the genetic defects leading to mitochondrial disorders, few of their pathogenetic mechanisms are fully understood.
In particular, the relationship between the presence of an activity defect in a given OXPHOS 1 complex and its effect on mitochondrial energy production remains problematic. Indeed, several authors have showed 20411 trainerhandbook it was possible to inhibit the activity of various OXPHOS complexes, up to a critical value, without affecting the rate of mitochondrial respiration or ATP synthesis 3.
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It partially controls the phenotypic expression of OXPHOS defects and therefore contributes to the variability in the clinical presentation of mitochondrial disorders. It 20411 trainerhandbook also been reported that a variation in the biochemical threshold value between tissues explains part of the tissue 20411 trainerhandbook observed in mitochondrial diseases 5.
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Thus, finding the molecular 20411 trainerhandbook that determine the threshold value and its variability will contribute to a better understanding of the pathogenesis of mitochondrial cytopathies and 20411 trainerhandbook to design new therapeutic approaches 6. In this study, we tested the hypothesis that the biochemical threshold effect resulted from the mobilization of a pool 20411 trainerhandbook inactive OXPHOS enzymes.
We also analyzed how this process varied in different tissues, enzyme isoforms, or respiratory steady states.
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Our study focused on the adenine nucleotide translocator ANT because it is possible to quantify the functional carriers participating actively in respiration using CATR 8 - 11an irreversible tight binding inhibitor of ANT 12 that binds only to the active form 13 Our 20411 trainerhandbook give the first molecular explanations for the biochemical threshold effect, based on the excess of activity provided by either 1 a mobilization of inactive ANT1 subunits that assemble into new oligomeric active carriers or 2 conformational changes in ANT1 in a permeability transition pore-like structure.
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